Rapid handheld continuous electroencephalogram (eeg) has the potential to detect delirium in older adults

Background: Delirium-related biochemical derangements lead to electrical changes that can be detected in electroencephalographic (EEG) patterns followed by behavioral signs and symptoms. Studies using limited lead EEG show a large difference between patients with and without delirium while discriminating delirium from other causes. Handheld rapid EEG devices may be capable of detecting delirium before symptom onset, thus providing an objective physiological method to detect delirium when it is most amenable to interventions. Objective: The aimof this studywas to explore the potential for rapid EEG to detect waveform pattern changes consistent with delirium status. Methods: This prospective exploratory pilot study used a correlational design and mixed models to explore the relationships between handheld portable EEG data and delirium status. Results: While being under powered minimized opportunities to detect statistical differences in EEGderived ratios using spectral density analysis, sleep-to-wake ratios tended to be higher in patients with delirium. Conclusions: Limited lead EEG may be useful in predicting adverse outcomes and risk for delirium in older critically ill patients. Although this population is at the highest risk for mortality, delirium is not easily identified by current clinical assessments. Therefore, further investigation of limited lead EEG for delirium detection is warranted. © 2022 Lippincott Williams and Wilkins. All rights reserved

Immunoactivation and immunopathogeny during active visceral leishmaniasis Imunoativação e imunopatogenia durante leishmaniose visceral ativa

Visceral leishmaniasis is caused by protozoan parasites of the Leishmania donovani complex. During active disease in humans, high levels of IFN-&#947; and TNF-&#945; detected in blood serum, and high expression of IFN-&#947; mRNA in samples of the lymphoid organs suggest that the immune system is highly activated. However, studies using peripheral blood mononuclear cells have found immunosuppression specific to Leishmania antigens; this poor immune response probably results from Leishmania antigen-engaged lymphocytes being trapped in the lymphoid organs. To allow the parasites to multiply, deactivating cytokines IL-10 and TGF-&#946; may be acting on macrophages as well as anti-Leishmania antibodies that opsonize amastigotes and induce IL-10 production in macrophages. These high activation and deactivation processes are likely to occur mainly in the spleen and liver and can be confirmed through the examination of organ samples. However, an analysis of sequential data from studies of visceral leishmaniasis in hamsters suggests that factors outside of the immune system are responsible for the early inactivation of inducible nitric oxide synthase, which occurs before the expression of deactivating cytokines. In active visceral leishmaniasis, the immune system actively participates in non-lymphoid organ lesioning. While current views only consider immunocomplex deposition, macrophages, T cells, cytokines, and immunoglobulins by diverse mechanism also play important roles in the pathogenesis.<br>A leishmaniose visceral é causada por protozoários do gênero do complexo Leishmania donovani. Durante a doença ativa no homem são detectados altos níveis de IFN-&#947; e de TNF-&#945; no soro, e elevada expressão de mRNA de IFN-&#947; em amostras de órgãos linfóides sugerindo um estado intensamente ativado do sistema imunológico. A visão atual, no entanto, refere-se à imunossupressão específica aos antígenos de Leishmania com base em estudos utilizando células mononucleares do sangue periférico; a explicação para sua resposta deficiente seria provavelmente porque os linfócitos compometidos com antígeno de Leishmania são sequestrados nos órgãos linfóides. Para permitir a proliferação do parasito, citocinas desativadoras IL-10 e TGF-&#946; atuariam nos macrófagos, bem como os anticorpos anti-Leishmania opsonizando amastigotas e induzindo a produção IL-10 pelos macrófagos. Estes processos de intensa ativação e desativação provavelmente ocorreriam no baço e fígado, principalmente, e confirmados com amostras de órgãos. No entanto, analisando dados seqüenciais obtidos na leishmaniose visceral no hamster, sugere-se provável presença de fatores fora do sistema imunológico como responsável pela inativação inicial de sintase induzível do óxido nítrico que ocorre antes da expressão de citocinas desativadoras. Na leishmaniose visceral ativa o sistema imunológico participa ativamente na lesão de órgãos não linfóides. Contrária à visão existente que considera somente mecanismos de deposição de imunocomplexos, observa-se na patogenia a participação de macrófagos, células T, citocinas e imunoglobulinas por mecanismo alternativo